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CHEST PAIN 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
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1  Introduction 
Chest pain is a very common complaint and often creates fear, for sufferers and 
relatives, of serious heart or lung disease.  Accurate diagnosis depends mainly on a 
careful history of the site and radiation of the pain, its character and duration, 
together with aggravating and relieving factors, aided by physical examination and 
special investigations. 
 
Chest pain can be classified as central (including precordial) and lateral, each 
category being subdivided into acute, usually presenting as an emergency, and 
chronic – of days’ or weeks’ duration at presentation.  In terms of disability analysis, 
chronic chest pain is far more common and important, so the causes of this will be 
described before the acute causes. 
 
For completeness, a brief account will be given first of the causes of superficial 
chest pain.  Ischaemic heart disease (IHD), including myocardial infarction (MI), 
angina, unstable angina and other variants, is described (with differential diagnoses) 
in a separate protocol.  The differential diagnoses for each condition, apart from 
IHD, are the others described in the same section. 
 
In most cases of chest pain, especially if chronic, taking a careful history will indicate 
the likely correct diagnosis.  The features of angina and MI that differentiate them 
from non-cardiac chest pain are described in the IHD protocol. 
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2  Superficial Chest Pain 
Most varieties of superficial chest pain are due to infection and inflammation, and 
are obvious on examination. 
2.1  Viral 
 
Herpes zoster, causing shingles, involves thoracic nerve roots in at least 50% of 
cases.  Pain and paraesthesiae may occur for a few days before the eruption 
appears.  Vesicles, on an erythematous base, are unilateral and occupy the area of 
one or more dermatomes.  Some patients have fever, malaise and axillary node 
enlargement in the acute phase.  The lesions form scabs and heal in 1-2 weeks, 
without scarring unless they have become secondarily infected.  Particularly in the 
elderly, post-herpetic neuralgia may occasionally cause severe pain for a long time 
after the eruption has disappeared, which may cause some functional disability. 
2.2  Bacterial 
 
Superficial inflammation may have spread from a deeper lesion such as an 
empyema. 
2.3  Phlebitis 
 
In  Mondor’s disease, phlebitis of the subcutaneous anterior thoracic veins causes 
either pleuritic-type pain or pain on raising the arms.  The inflamed vein may be 
palpable as a tender cord.  Resolution occurs within 1-2 months. 
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3  Chronic Central Chest Pain 
The most important cause of central chest pain is ischaemic heart disease (IHD): 
this causes stable angina, unstable angina and myocardial infarction, which are 
described in a separate protocol.  Causes of chronic central chest pain other than 
stable and unstable angina are discussed below. 
3.1  Pain Of Oesophageal Origin 
3.1.1 
Description 
 
Pain from the oesophagus is felt in the midline of the chest with radiation to the jaw, 
back, shoulders and possibly the inner arms.  There may be an inconsistent 
relationship to exertion – mimicking angina.  The pain characteristically wakes the 
patient in the early hours of the morning. 
 
3.1.1.1 
Aetiology 
 
The pain may be due to isolated oesophageal spasm, developing achalasia of the 
cardia, or hiatus hernia with reflux and oesophagitis (in which heartburn is 
characteristic – sternal pain radiating upwards from the xiphoid).  Acid reflux into the 
oesophagus may reduce coronary blood flow reserve to the point of inducing true 
angina (linked angina). 
 
3.1.1.2 
Prevalence 
 
Gastro-oesophageal reflux occurs to some degree in everybody, but is only 
considered a disease when it causes significant symptoms or complications.  
Idiopathic achalasia has an annual incidence of about 1-2/200,000. 
3.1.2 
Diagnosis 
 
3.1.2.1 
Clinical features 
 
The pain is associated with taking food (often only certain foods), temporarily 
relieved by belching or swallowing saliva, and often worse in postures favouring 
regurgitation – lying, bending forward or driving a small car, especially with a tight 
seat belt.  The dyspepsia is relieved by antacids. 
 
3.1.2.2 
Investigations 
 
 Endoscopy. 
  Reproduction of the pain by instillation of dilute hydrochloric acid into the lower 
oesophagus. 
  24-hour pH monitoring used occasionally. 
  Barium swallow – BUT most hiatus herniae are asymptomatic so this finding 
does not exclude myocardial ischaemia.  Trial of omeprazole may be 
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diagnostically useful and has practical and economic advantages over 
sophisticated investigations. 
3.1.3 
Treatment 
 
Antacids, H2 antagonists, proton pump inhibitors and motility promoters. 
Confusingly, the pain of oesophageal dysmotility can, like angina, be relieved by 
nitrates or calcium antagonists. 
3.1.4 
Prognosis 
 
Prognosis depends on the exact nature of the oesophageal disorder. 
3.1.5 
Main Disabling Effects 
 
The disabling effects depend on the efficacy of medical and surgical treatment and 
should be minimal.  However, as with other conditions described in this protocol, 
disability analysts may see people whose disease has not been optimally managed, 
or whose condition has not responded to best current therapy – such factors may 
increase the degree and duration of disability, leading to time off work in some 
cases. 
3.2  Other Gastrointestinal Conditions 
3.2.1 
Gastric Distension 
 
Gastric distension (often due to aerophagy) can cause substernal discomfort. 
3.2.2 
Peptic Ulcer 
 
The relationship of peptic ulcer pain to meals, or lack of food, is important. 
3.2.3 
Gallbladder Disease 
 
The pain of gallbladder disease is often related to eating fatty foods.  Gallbladder 
disease and ischaemic heart disease are both common, so they often co-exist – 
whether more often than by chance remains a matter of debate.  ST/T wave 
changes and a response to nitrates may occur with cholecystitis.  Gallbladder pain 
can radiate into the front of the chest and simulate angina, but even in the presence 
of gallbladder disease, central chest pain with a constant relationship to exertion 
must be regarded as angina, until proved otherwise. 
3.2.4 
Chronic Relapsing Pancreatitis 
 
The recurrent epigastric and left upper abdominal quadrant pain often radiates to the 
back and sometimes to the central anterior chest.  The attack frequency may cause 
the pain to become almost continuous; the pain can be very severe, so medical 
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attention may be sought.  Diabetes mellitus and/or pancreatic insufficiency may 
develop; the latter results in malabsorption, loss of weight and steatorrhoea – 
impaired digestion of fat and protein leading to the passage of bulky fatty stools with 
heavy nitrogen loss. 
3.2.5 
Investigations 
 
Endoscopy, Ba swallow and meal, cholecystogram, serum amylase and stomach 
acid secretion studies help to clarify the diagnosis.  X-ray often shows calcification in 
chronic pancreatitis. 
3.2.6 
Treatment 
 
Once the correct diagnosis has been established, routine management applies. 
3.2.7 
Prognosis and Main Disabling Effects 
 
The prognosis and main disabling effects are determined by the nature of the 
underlying gastrointestinal disorder.  Chronic pancreatitis is the most likely condition 
to cause long-term debility. 
3.3  Musculoskeletal Causes 
3.3.1 
Recurrent Mild Trauma 
 
This may be related to occupation (or a leisure pursuit), is often a dull ache to the 
side of the midline, and may correlate with particular movements – especially if 
anterior thoracic muscles are the sites of origin. 
3.3.2 
Spondylosis or Spondylitis 
 
Pain from thoracic or even cervical spondylosis can be referred to the anterior chest, 
simulating angina.  There is usually some limitation of spinal movement, often 
muscle weakness and sometimes reduced or absent arm reflexes.  The distribution 
of the pain often corresponds to that of one or more dermatomes.  Radiological 
proof of spondylosis does not exclude angina, but relief of the pain by wearing a 
cervical collar provides good evidence of a skeletal origin. 
Chronic mild trauma to interspinous ligaments (e.g. in scoliosis) may be a cause of 
otherwise unexplained precordial pain. 
Ankylosing spondylitis can cause diffuse anterior chest wall pain, often associated 
with local tenderness over the sternum and costal cartilages. 
3.3.3 
Less Common Musculoskeletal Conditions 
 
3.3.3.1 
Tietze’s syndrome 
 
Tietze’s syndrome causes pain of sudden or gradual onset in one or more upper 
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costal cartilages.  The pain is worse on deep breathing or coughing and the affected 
cartilage is swollen and tender. 
 
3.3.3.2 
Xiphoidalgia 
 
Xiphoidalgia is a similar condition involving the xiphisternum, which may be related 
to recurrent mild trauma. 
 
3.3.3.3 
Sternal Pain 
 
Pain arising in the sternum itself may be due to myelomatosis, metastases, 
ankylosing spondylitis, osteomyelitis or fracture (usually pathological). 
 
3.3.3.4 
Precordial catch 
 
Precordial catch causes sudden sharp pain at or near the cardiac apex, which 
occurs while seated and lasts for a few minutes only, being relieved by a single, 
painful deep inspiration. 
3.3.4 
Treatment and Prognosis 
 
Treatment and prognosis are those of the underlying disorder. 
3.3.5 
Main Disabling Effects 
 
With appropriate treatment these conditions should not cause significant long-term 
disability (unless, rarely, a regional pain syndrome develops). 
3.4  Non-coronary Cardiac Pain 
3.4.1 
Prolapsed Mitral Valve Cusp 
 
Prolapsed mitral valve cusp is a relatively common lesion, which is often associated 
with a mid-systolic click and late systolic murmur.  The pain is very variable in site, 
duration and severity and has no clear-cut diagnostic features.  Diagnosis is 
confirmed by echo- or angio-cardiography. 
3.4.2 
Pulmonary Hypertension and Pulmonary Stenosis 
 
Chronic pulmonary hypertension (PHT), either primary or secondary (as in mitral 
stenosis or the Eisenmenger syndrome), can produce a pain indistinguishable from 
angina.  The cause is probably myocardial right ventricular ischaemia resulting from 
severely limited cardiac output and/or excessive right-sided systolic load with severe 
PHT.  When advanced, other features of PHT may include: - dyspnoea; syncope on 
exertion; oedema; poor peripheral circulation (cold extremities); central and/or 
peripheral cyanosis; elevated JVP; sinus tachycardia or atrial fibrillation; 3rd (right 
ventricular) or 4th heart sounds; a loud pulmonary 2nd sound; tricuspid regurgitation; 
sometimes a lowered systemic BP; and, possibly, hepatomegaly and ascites. 
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Severe pulmonary stenosis can cause a similar pain. 
3.5  Chronic Respiratory Disease 
 
Dyspnoea, especially when associated with airways obstruction, may be described 
as “tightness in the chest”, so that leading questions may result in the label of a 
“tight pain” across the chest and hence an erroneous diagnosis of angina. 
3.6  Psychological Conditions 
3.6.1 
Da Costa’s Syndrome 
 
Chronic anxiety is the commonest underlying disorder in Da Costa’s syndrome 
(synonyms: neurocirculatory asthenia; effort syndrome; soldier’s heart; cardiac 
neurosis; disordered action of the heart). 
 
3.6.1.1 
Diagnosis 
 
The other features are chest pain, dyspnoea, palpitations, fatigue, dizziness, sighing 
and hyperventilation.  The pain is most common in the left submammary region, but 
may be nearer the midline or anywhere on the left side of the chest, even radiating 
to the left arm.  In character it is composed of sharp stabbing twinges superimposed 
on a background dull ache that persists for many hours.  The important point 
distinguishing it from angina is that the pain often occurs after, rarely during, 
exertion.  It is not normally relieved by anti-anginal medication.   
 
3.6.1.2 
Aetiology 
 
The mechanism of the pain is unknown, but it is sometimes triggered by a minor 
musculoskeletal abnormality.  The pain convinces the patient that his heart is 
diseased and is perpetuated by the anxiety thus engendered. 
 
3.6.1.3 
Treatment and prognosis 
 
Hence the condition responds best to a confident diagnosis with firm reassurance; it 
can be aggravated by unnecessary investigation, which tends to increase concern 
rather than ameliorate it. 
 
3.6.1.4 
Main disabling effects 
 
Properly managed, Da Costa’s syndrome should not be a cause of long-term 
disability. 
3.6.2 
Psychological Problems in Patients with Non-cardiac Chest Pain 
 
Atypical non-cardiac chest pain is common and disabling, often persisting despite 
negative investigations; fundamental factors include inappropriate health beliefs and 
the continued misinterpretation of minor physical symptoms as evidence of heart 
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disease.[1]  Patients with non-cardiac chest pain often display illness behaviour.  
Summaries of papers describing follow-up and psychological treatment for various 
groups of patients with non-cardiac chest pain are given at Appendix A. 
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4  Chronic Lateral Chest Pain 
Almost all the tissues of the lateral chest wall (pleura, muscles, ribs and intercostal 
nerves) can be the sites of painful lesions. 
4.1  Pathology involving the Intercostal Nerves 
4.1.1 
Spinal Disease 
 
Spinal disease can cause referred chest pain anterolaterally. 
4.1.2 
Nerve Root Compression 
 
Nerve root compression can occur in: 
 
 
Pathological fracture of the thoracic spine. 
 Tuberculosis. 
 
Spondylosis with disc protrusion (uncommon in the thoracic spine). 
 
Neurofibromatosis (does not often cause pain). 
4.1.3 
Mononeuritis, Mononeuritis Multiplex and Polyneuritis 
 
Diabetes mellitus can cause a mononeuritis, mononeuritis multiplex (involvement of 
2 or more peripheral nerves, though less than a polyneuritis), or a true polyneuritis; 
each of these may lead to asymmetric chest pain. 
 
Alcoholic poisoning, polyarteritis nodosa and leprosy can cause mononeuritis 
multiplex or polyneuritis. 
4.1.4 
Tabes Dorsalis 
 
Tabes dorsalis is one manifestation of late neurosyphilis, presenting 10 – 25 years 
after primary infection with Treponema pallidum.  The characteristic “lightning pains” 
can occasionally involve the chest, being “needle-like“ or “knife-like”, the sudden 
stabbing nature invariably being illustrated by gesture.  Usually only one area is 
affected at any time and the zone involved often remains tender for a while.  The 
bouts occur irregularly and tend to be provoked by damp weather.  Other symptoms 
include visual and sphincter disturbances, impotence, ataxia (wide stamping gait, 
worsened by eye closure), gastric or other tabetic crises and trophic lesions (e.g. 
arthropathies and perforating foot ulcers).  Examination may reveal: Argyll-
Robertson pupils (small, irregular, fixed to light but contracting on accommodation-
convergence), ptosis and optic atrophy; loss of knee/ankle jerks and 
vibration/position/deep pain sensation in the legs; also Charcot’s joints – painless 
and unusually mobile despite the gross pathology.  Penicillin treatment in the early 
stages reverses the disease, but delay makes progressive changes only partially 
reversible.  Symptomatic treatment may be needed for confusion, ataxia, Charcot 
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joints, urinary retention and lightning pains.  Tabes dorsalis is now rare in the UK. 
4.2  Aortic Aneurysm 
 
Aortic aneurysms can be either ‘true’, with intact aortic wall, or ‘false’ – a contained 
rupture (with the wall being made up of adventitia and peri-aortic fibrous tissue) - 
following previous trauma (aortic transection) or chronic dissection. 
4.2.1 
Aneurysm of the Ascending Aorta 
 
Aneurysm of the ascending aorta may erode the sternum, thus causing chest pain 
(which may radiate to the neck and jaw), but much more often causes no symptoms 
at all.  It is thought to be due to an abnormality of medial connective tissue, which 
can be either: - idiopathic; part of Marfan’s or Reiter’s syndrome; or a feature of 
rheumatoid disease, giant cell arteritis or syphilitic aortitis. 
4.2.2 
Aneurysm of the Arch and Descending Aorta 
 
Aneurysm of the arch and descending aorta can erode vertebrae and lead to nerve 
root pressure, causing very severe pain, which may radiate to the interscapular 
area.  Aortic root dilatation may result in aortic regurgitation. 
4.2.3 
Pressure on Mediastinal Structures 
 
Pressure on mediastinal structures causes symptoms and signs as follows: 
 
 
Left recurrent laryngeal nerve – left vocal cord paralysis and hoarseness. 
 
Trachea – cough and stridor. 
 
Oesophagus – dysphagia. 
 
Left main bronchus – collapse of the left lung and infection; there may be a 
tracheal tug. 
4.2.4 
Imaging Techniques 
 
 
Plain CXR may suggest the diagnosis. 
 
MRI and CT scans are the investigations of choice and can monitor post-
operative follow-up. 
 
Contrast aortography now superseded by the above. 
4.2.5 
Treatment 
 
 
Surgical repair using synthetic graft, because of risk of rupture. 
 
5 - 50% mortality – greatest risk for aneurysms of the aortic arch. 
 Morbidity: 

(a) 
Neurological - paraplegia/paraparesis if descending thoracic. 
 
 
- cerebral if aortic arch involved. 
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(b) Renal failure - after repair of descending thoracic or 
thoracoabdominal aorta. 
4.2.6 
Prognosis 
 
10-year survival around 40%.  Re-operation may be needed for aneurysmal 
dilatation at the site of anastomosis between synthetic graft and native aorta. 
4.3  Intrathoracic Malignant Disease 
 
Intrathoracic malignant disease (primary or secondary) may cause pain in various 
ways: 
4.3.1 
Bronchial Carcinoma 
 
Bronchial carcinoma leads to pleural pain caused by: 
 
 
Direct invasion of the pleura, often with effusion. 
 
Lung infection distal to a blocked bronchus. 
4.3.2 
Primary Tumours of the Pleura 
 
Primary tumours of the pleura (e.g. mesothelioma) can either: 
 
 
Cause pleuritic pain directly, or 
 
Involve ribs and intercostal nerves producing severe pain. 
4.3.3 
Metastases in the Thoracic Spine 
 
Metastases in the thoracic spine can cause intercostal pain. 
4.3.4 
Metastases in the Ribs 
 
Metastases in the ribs can be extremely painful. 
4.3.5 
Mediastinal Tumours 
 
Mediastinal tumours can cause poorly localised (sometimes lateral, though often 
central) chest pain without other pressure symptoms. 
4.3.6 
Treatment and Prognosis 
 
As well as analgesia, treatment may involve surgery, radiotherapy and/or 
chemotherapy.  Particularly if secondaries are the cause of pain, the prognosis is 
likely to be poor – in which case treatment may be palliative. 
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5  Acute Central Chest Pain 
The most important cause of central chest pain is ischaemic heart disease (IHD) 
causing stable angina, unstable angina and myocardial infarction (MI) - these are 
described in a separate protocol.  Causes of acute central chest pain other than MI 
are discussed below. 
5.1  Pericarditis 
5.1.1 
Description 
 
5.1.1.1 
Aetiology 
 
Localised pericarditis is common in myocardial infarction.  Other less common 
causes are: 

Viral (often Coxsackie B), bacterial, fungal and parasitic infections

Connective tissue disorders – SLE, rheumatic fever, rheumatoid 
disease or systemic sclerosis. 

Dressler’s  (post-MI)  and other similar syndromes - (e.g. post-
cardiotomy)

Chronic renal failure/uraemia. 

Untreated hypothyroidism. 

Malignancy. 

Idiopathic – usually sporadic, but may occur in outbreaks (some 
patients develop myocarditis). 
 
5.1.1.2 
Prevalence 
 
Except for the acute idiopathic form, the prevalence is related to those of the 
underlying conditions. 
5.1.2 
Diagnosis 
 
5.1.2.1 
Clinical features 
 
(a) Pain  -  in, and to the left of, the sternal region, which may radiate to the 
epigastrium, neck, back, shoulders and, occasionally, to the arms.  Severity 
varies from mild discomfort to extreme agony; described as "stabbing” or “knife-
like” - so it mimics the pain of myocardial ischaemia
 
Aggravated by: coughing; deep breathing; twisting movements (e.g. turning over 
in bed); hyperventilation associated with exertion; recumbent (supine) position; 
and swallowing.  Relieved by sitting up/forwards. 
 
(b) Friction pericardial rub – high-pitched scratching sound, audible throughout the 
cardiac cycle; intensity varies with position – often evanescent.  A pericardial 
effusion 
may develop – detectable on echocardiography
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(c)  Fever and systemic upset. 
 

5.1.2.2 
ECG 
 
 
S-T elevation, concave upwards, in all standard leads except aVR. 
 
Later, over 2 – 3weeks, T-wave inversion (again mimicking myocardial 
ischaemia). 
 
5.1.2.3 
Virology/serology/renal or thyroid function tests 
 
 
To detect/confirm underlying cause. 
5.2  Dissecting Aortic Aneurysm 
5.2.1 
Description 
 
Acute aortic dissection is a catastrophic disorder often leading to sudden death.  A 
tear in the aortic intima allows it to be dissected or stripped from its subintimal 
layers, destroying the tunica media.  Involvement of the ascending aorta influences 
prognosis and management, so the Stanford classification divides dissections into 
Type A, involving the ascending aorta, and Type B, in which the ascending aorta is 
spared. 
 
5.2.1.1 
Aetiology 
 
There is weakness of the aortic media with breakdown of elastic and collagen 
tissues (cystic degeneration).  Age-related degeneration, perhaps accelerated by 
hypertension, is the commonest process, but Marfan’s, Ehlers-Danlos and Noonan 
syndromes are complicated by aortic dissection because of their effect on 
connective tissue.  Occasionally, dissection follows disruption of atheromatous 
plaque or aortic arteritis. 
 
5.2.1.2 
Prevalence/Incidence 
 
Patients are usually in the 6th or 7th decade of life and two-thirds are males. 
5.2.2 
Diagnosis 
 
5.2.2.1 
Clinical features 
 
 
Very severe “tearing” anterior chest pain (hardly influenced by opiates) 
radiating to the neck, interscapular area and (later) the abdomen; it rarely 
spreads to the arms.  With thoracic aortic dissection, the pain may begin in the 
back. 
 
Nausea, vomiting, profuse sweating and syncope. 
 
One or more peripheral pulses may be absent (or disappear while under 
observation). 
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 
Other evidence of arterial occlusion (e.g. hemiparesis, blindness in one eye, 
myocardial ischaemia or haematuria). 
 
Aortic regurgitation (if the aortic ring is involved) – indicates a Type A 
dissection. 
 
Rupture into the pericardium or pleural space may cause acute tamponade or 
pleural effusion. 
 
In the absence of tamponade, BP little changed or raised – whereas usually 
lowered in MI. 
 
5.2.2.2 
Investigations 
 
 
ECG – normal unless a coronary artery is involved or pre-existing 
hypertensive changes are present. 
 
Radiography – on CXR, not easy to distinguish dilatation of dissection from 
unfolding of the aorta without a previous film. 
 
MRI is the investigation of choice, if available, otherwise: 
 
CT scan, aortography or transoesophageal echocardiography. 
5.2.3 
Treatment 
 Adequate 
analgesia. 
 
Rigorous control of hypertension (avoiding ACE inhibitors because of possible 
extension of the dissection to involve the renal arteries), both initially and long-
term. 
 
Emergency surgery (within 24 hours) improves survival for Type A dissections, 
and may be necessary for complications of Type B dissections (e.g. vital organ 
compromise – kidney or intestine, haemorrhage, or evidence of extension). 
5.3  Massive Pulmonary Embolism 
5.3.1 
Description 
 
Acute major pulmonary embolism results from significant obstruction to the proximal 
pulmonary arteries. 
 
5.3.1.1 
Aetiology 
 
Embolism from thrombosis in the pelvic or deep leg veins.  Predisposing factors: 
 
Postoperative period and/or major trauma. 
 Enforced 
recumbency: 
  Low cardiac output (e.g. post-MI, cardiac failure). 
  Probably, (economy-class) long-haul air travel – much current debate. 
 
Female sex hormones 
 
Pregnancy, oral contraceptive pill or HRT. 
 
Hypercoagulability and hyperviscosity syndromes. 
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 
Malignancy, increasing age, obesity and smoking. 
 
5.3.1.2 
Incidence 
 
An analysis of death certificates in England and Wales in 1967 revealed 4981 
reports in which pulmonary embolism was the suspected primary cause of death, 
but the number increased to 21,000 when more than one cause had been recorded. 
 Many patients die with  rather than from emboli, particularly the elderly with 
malignancy or chronic cardiac/lung disease.  Pulmonary embolism was considered 
to have been the sole cause of death in only 7% of adults dying in a district general 
hospital, though it had contributed towards death in another 7%.  The true incidence 
of pulmonary embolism may be rising as hospital patients become older and less 
mobile over the decades.[2] 
 
Between 300,000 and 600,000 patients suffer a pulmonary embolism in the USA 
each year, with a mortality of 30% if untreated and 3-8% with treatment. 
5.3.2 
Diagnosis 
 
5.3.2.1 
Clinical features 
 
Rapid severe illness with: 
 
 
Central chest pain, nearly identical to that of MI. 
 
Severe breathlessness, tachypnoea and rapid pulse. 
 
Faintness or loss of consciousness. 
 Peripheral 
cyanosis. 
 
Very low BP and very raised JVP. 
 
Gallop rhythm over right ventricle. 
 
With peripheral emboli: - pleuritic pain, pleural rub and haemoptysis. 
 
5.3.2.2 
Investigations 
 
 
CXR – dilatation of one or both branches of the pulmonary artery. 
 
Pulmonary angiography – shows occlusion of the pulmonary artery. 
 
ECG – simulates changes of antero-inferior infarction, right axis deviation and 
clockwise rotation. 
 
V/Q scan or spiral CT
5.3.3 
Treatment 
 
 Emergency 
hospital 
admission. 
 
Tilt head-down and oxygen. 
 
CVP line to monitor venous pressure and give IV colloid, inotropes and 
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thrombolytic agents - streptokinase, urokinase or tissue plasminogen activator 
(tPA) – and possibly hydrocortisone. 
 
Thermodilution pulmonary artery catheter – to monitor cardiac output, 
pulmonary artery pressure and mixed venous oxygen saturation, facilitating 
assessment of the rate of resolution of the embolus in response to treatment. 
5.3.4 
Prognosis 
 
High early mortality, so vigorous therapy should be pursued. 
5.4  Respiratory Disease 
5.4.1 
Tracheitis 
 
Tracheitis causes upper sternal pain aggravated by the hyperventilation of exercise 
(so may mimic angina).  Persistent coughing can lead to soreness in the upper 
airways and trachea. 
5.4.2 
Mycoplasma pneumonia 
 
Mycoplasma pneumonia is never associated with pleurisy, but may cause a 
substernal pain aggravated by coughing. 
5.5  Gastrointestinal Disease 
 
Upper abdominal catastrophes, such as perforated peptic ulcer and acute 
pancreatitis can cause pain felt in the midline of the front of the chest.  Abdominal 
signs, and gas under the diaphragm on X-ray or a raised serum amylase, confirm 
the respective diagnoses. 
5.6  Pericardial Fat Necrosis 
 
Pericardial fat necrosis is a rare cause of chest pain simulating that of pericarditis.  
There is no friction rub and the ECG is normal.  CXR may reveal a para-cardiac 
mass. 
5.7  Acute Anxiety 
 
In a genuine and terrifying panic attack the patient complains of dizziness, 
palpitations, dyspnoea and precordial oppression or pain.  “Angor animi” (the fear of 
impending death) is more prominent than in actual myocardial ischaemia, and 
exacerbates the anxiety.  The circumstances of the attack and total absence of 
objective evidence of organic disease should clarify the diagnosis. 
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6  Acute Lateral Chest Pain 
6.1  Pleurisy 
6.1.1 
Description 
 
Pleurisy is pain related to respiration. 
 
6.1.1.1 
Aetiology 
 
 
Pulmonary infections (e.g. lobar pneumonia, tuberculosis). 
 
Vascular lesions (e.g. pulmonary infarction). 
 
Connective tissue disorders (e.g. SLE). 
 
6.1.1.2 
Incidence 
 
The incidence of pleurisy is dependent on those of the underlying conditions. 
6.1.2 
Diagnosis 
 
6.1.2.1 
Clinical features 
 
(a) 
Pain in the cutaneous areas supplied by the intercostal nerves (which supply 
plentiful pain fibres to the parietal pleura), including a large part of the anterior 
abdominal wall.  Spasm of the intercostal muscles may be a contributory 
factor. 
 
Sharp, superficial, of variable severity. 
 
Aggravated by deep breathing and coughing. 
 
Exacerbated or relieved by change of posture. 
 
Relieved completely by holding the breath in expiration. 
 
Inspiration abruptly halted by pain, so that respiration is often very 
shallow. 
 
Pain of diaphragmatic pleurisy referred to the shoulder (a common 
feature of sub-diaphragmatic lesions – e.g. liver or subphrenic abscess). 
 
(b) 
Pleural friction rub – a characteristic creaking sound (like that of rubbing 
leather): 
  Present during inspiration and expiration. 
  Poorly correlated to the pain. 
 
 
(c) 
Pleural effusion – development of this usually abolishes the pain and the 
pleural rub. 
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6.1.2.2 
Investigations 
 
CXR and sputum culture. 
6.1.3 
Treatment and Prognosis 
 
Treatment and prognosis are those of the underlying cause. 
6.2  Bornholm Disease 
6.2.1 
Description 
 
Synonyms: - epidemic pleurodynia/myalgia; Devil’s grip. 
 
6.2.1.1 
Aetiology 
 
Bornholm disease is due to Group B Coxsackie viruses. 
 
6.2.1.2 
Incidence 
 
Bornholm disease occurs sporadically or in outbreaks, affecting mainly children or 
young adults.  In large temperate urban conurbations, outbreaks generally occur in 
summer or autumn. 
6.2.2 
Diagnosis 
 
6.2.2.1 
Clinical features 
 
 
Acute onset, the intercostal muscles being most often affected. 
 
Pain is the presenting symptom and may be extremely severe. 
 
Respiration becomes shallow, rapid and painful. 
 
Fever quickly develops; then headache and malaise are common. 
 
The affected muscles are tender and there may be a pleural rub plus a 
lymphocytosis. 
 
The disease lasts 7 - 10 days, so recovery is usually rapid, but relapses are 
frequent and may continue for several weeks. 
 
However, no serious complications or deaths have been reported and 
treatment is symptomatic. 
 
There should be no long-term disability. 
6.3  Trichinosis 
 
In trichinosis, involvement of the intercostal muscles can produce pleuritic pain.  The 
diagnosis is supported by finding peri-orbital or generalised oedema and by blood 
eosinophilia. 
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6.4  Splenic Pain 
 
Pain arising from the capsule of the spleen is related to respiration and commonly 
due to splenic infarction.  There may be a friction rub resembling that of pleurisy.  
Splenic pain may occur in Hodgkin’s disease and similar conditions. 
6.5  Spontaneous Pneumothorax 
6.5.1 
Description 
 
6.5.1.1 
Aetiology 
 
A pneumothorax results from gas entering the potential space between the visceral 
and parietal pleura.  A spontaneous pneumothorax is caused by rupture of a bulla or 
cyst on the surface of the lung. 
 
6.5.1.2 
Incidence 
 
The annual incidence is about 9 per 100,000.  It is more common in asthmatics and 
also in young men, with a male:female ratio of approximately 4:1.  About 20% of 
patients who have had one pneumothorax are likely to have a recurrence. 
6.5.2 
Diagnosis 
 
6.5.2.1 
Clinical features 
 
(a) Pain  
 
  Usually abrupt in onset and pleuritic in type. 
  Some patients complain of a dull ache or a sense of tightness. 
  A few have no pain at all. 
  Central chest pain may be caused by dissection of air into the 
mediastinum with an audible “crunching” sound over the heart. 
 
(b) Physical 
signs 
  Reduced chest wall movement and breath sounds on the affected side. 
  Hyper-resonant percussion note on the affected side. 
  If under tension, deviation of the trachea to the normal side. 
  Auscultation may detect the same “crunching” sound. 
 
6.5.2.2 
Investigations 
 
CXR with expiratory film. 
 
6.5.2.3 
Treatment 
 
Chest drain or aspiration. 
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6.6  Trauma 
 
Fractured ribs. 
 
 
Typical history of appropriate trauma. 
 Localised 
tenderness. 
 
Visible on CXR, either immediately or later after callus formation. 
 
Significant disability unlikely once sound union has occurred. 
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Appendix A - Psychological Treatment for Chest Pain 
Psychological Treatment for Atypical Non-cardiac Chest Pain 
 
In a randomised controlled trial cognitive behaviour therapy proved effective.  There 
were significant reductions in chest pain, limitations and disruption of daily life, 
autonomic symptom distress and psychological morbidity in the treated group.  The 
assessment-only control group were treated subsequently and showed comparable 
changes.  The improvements were maintained in both groups during 4 – 6 months’ 
follow-up.[3] 
Non-cardiac Chest Pain and Benign Palpitations in Cardiac 
Clinic Patients 
 
Patients referred from general practice to a hospital cardiac clinic with a presenting 
disorder of chest pain or palpitations were followed up for 3 years.  There were 39 
patients with a cardiac diagnosis and 51 with no cardiac or other major physical 
diagnosis.  The non-cardiac group was more likely to be young and female, and to 
report other physical symptoms and previous psychiatric problems. 
 
Both groups reported progressive improvement in presenting symptoms and 
disability, but little change in mental state.  Three quarters of the non-cardiac 
subjects described continuing limitation of activities, concern about the cause of their 
symptoms and dissatisfaction with medical care.  Outcome was poor for those who 
had negative investigations - despite reassurance that they had no cardiac disorder 
or other serious physical finding.[4] 
Psychosocial Outcome and Group Psychological Treatment 
in Patients with Chest Pain and Normal Coronary Arteries 
 
During assiduous 11-year follow-up of 46 patients with chest pain and normal 
coronary arteries, four died, one from IHD.  Chest pain continued in 74%, being 
frequent, severe or both in half of these, and led to further hospital treatment in 58%; 
13% had repeat coronary angiography.  Of the survivors, 71% were taking cardiac 
medication and 29% were unable to work for medical reasons.  High levels of chest 
pain, other physical symptoms, psychological distress and functional disability 
persisted long after angiography, (being similar to those found in patients with MI or 
angina) and led to heavy use of medical resources.[5] 
 
60 patients with continuing chest pain despite cardiological reassurance after normal 
angiography received small group psychological treatment in 6 sessions:  education; 
relaxation; breathing training; graded exposure to exercise; and challenging of 
automatic thoughts about heart disease.  Treatment reduced chest pain episodes 
from median 6.5 to 2.5 per week (p<0.01) and the prevalence of hyperventilation 
from 54% to 34% (p<0.01).  Improvements for anxiety and depression scores 
(p<0.05), disability rating (p<0.0001) and exercise tolerance (p<0.05) were 
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maintained after 6 months.  However, patients continuing to attribute their pain to 
heart disease had poorer outcomes.[6] 
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7  References 
1. 
Pearce MJ, Mayou RA, Klimes I.  The management of atypical non-cardiac 
chest pain.  Q J Med 1990; 76: 991-6. 
2. 
Ledingham JGG, Weatherall DJ.  Pulmonary embolism.  Chapter 15.26.  
Oxford Textbook of Medicine on CD-ROM.  Oxford University Press and 
Electronic Publishing B.V: 1996. 
3. 
Klimes I, Mayou RA, Pearce MJ, Coles L, Fagg JR.  Psychological treatment 
for atypical non-cardiac chest pain: a controlled evaluation.  Psychol Med 1990; 
20:  605-11. 
4. 
Mayou R, Bryant B, Forfar C, Clark D.  Non-cardiac chest pain and benign 
palpitations in the cardiac clinic.  Br Heart J 1994; 72: 548-53. 
5. 
Potts SG, Bass CM.  Psychosocial outcome and use of medical resources in 
patients with chest pain and normal or near-normal coronary arteries: a long-
term follow-up study.  Q J Med 1993; 86: 583-93. 
6. 
Potts SG, Lewin R, Fox KA, Johnstone EC.  Group psychological treatment for 
chest pain with normal coronary arteries.  Q J Med 1999; 92: 81-5. 
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8  Bibliography 
1.  Fleming PR.  Chest Pain.  In French’s Index of Differential Diagnosis (ed Bouchier IAD, 
Ellis H, Fleming PR).  Oxford:  Butterworth-Heinemann, 1996. 
2.  Gray HH,  Dawkins KD,  Morgan JM,  Simpson IA.  Lecture Notes on Cardiology, (4th 
edition).  Chapter 8 – Coronary Heart Disease.  Chapter 13 – The Pericardium.  Chapter 
15 – Diseases of the Aorta.  Chapter 16 – Pulmonary Hypertension and Pulmonary 
Thromboembolism.  Oxford: Blackwell Science, 2002. 
3.  (a) 
British Heart Foundation.  Factfile  02/1995.  Non-cardiac Chest Pain.  London, 
1995. 
 
(b) 
British Heart Foundation.  Factfile  05/2000.  Chest Pain – is it angina? 
 London, 2000. 
4.  (a) 
Swanton RH.  Stable and unstable angina.  Chapter 2.11. 
 
(b) 
Gibson DG.  Pericardial disease.  Chapter 2.26. 
 
(c) 
Ledingham JGG, Weatherall DJ.  Pulmonary embolism.  Chapter 2.30. 
 
(d) 
Benson MK.  Pleural disease.  Chapter 4.36. 
 
(e) 
Dent J.  Diseases of the oesophagus.  Chapter 5.3. 
 
(f) 
Greenwood RJ.  Neurosyphilis.  Chapter 13.28 
 
(g) 
Walton J.  Inflammatory myopathies.  Chapter 13.36. 
 All 
in 
Concise Oxford Textbook of Medicine  (ed Ledingham JGG, Warrell DA).  
Oxford University Press 2000. 
 
 
 
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